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PubMed2003

Left anterior descending coronary artery wall thickness measured by high-frequency transthoracic and epicardial echocardiography includes adventitia.

High-frequency, 2-dimensional transthoracic echocardiography (HR-2DTTE) measurements of the left anterior descending (LAD) coronary artery wall thickness are larger than measurements obtained by intravascular ultrasound. We hypothesize that this difference is due to inclusion of the third vascular layer, which may represent adventitia by HR-2DTTE, and that this layer must be increasing in thickness with the development of atherosclerosis. We evaluated the contribution of this third layer to the wall thickness of the normal and atherosclerotic LAD artery imaged by HR-2DTTE using high-frequency epicardial echocardiography (HFEE) as the reference standard. Eighteen patients (10 men, mean age 62 years), 13 with coronary atherosclerosis and 5 with normal coronary arteries, referred for open-heart surgery, underwent preoperative HR-2DTTE evaluation of the LAD artery (SONOS 5500; 3- to 8-MHz transducer) and intraoperative HFEE of the LAD artery (SONOS 5500; 6- to 15-MHz transducer). Wall thickness was greater in patients with coronary atherosclerosis than in those with normal coronary arteries by both HR-2DTTE (1.9 +/- 0.3 vs 1.0 +/- 0.1 mm, p = <0.001) and HFEE (1.8 +/- 0.2 vs 1.0 +/- 0.2 mm, p = <0.001). On HFEE, the average intima plus media thickness was greater in patients with coronary atherosclerosis than in those with normal coronary arteries (0.78 +/- 0.3 vs 0.34 +/- 0.1 mm, p = 0.005). The average thickness of adventitia was also greater in patients with coronary atherosclerosis than in those with normal coronary arteries (0.92 +/- 0.2 vs 0.54 +/- 0.2 mm, p = 0.0005). HR-2DTTE and HFEE measurements of the wall thickness correlated well (r = 0.83 [reader 1], p <0.001; r = 0.61 [reader 2], p <0.01). A third vascular layer, which likely included adventitia, represents a significant portion of the LAD wall thickness imaged by HR-2DTTE and HFEE, and it significantly increases in thickness with the development of atherosclerosis.

Adult↗
PubMed1996

Potential role of the adventitia in arteritis and atherosclerosis.

The role of the adventitia in vascular lesion formation has been largely ignored despite numerous studies which have suggested its potential importance. Adventitial reactions are common in atherosclerosis as well as arteritis. Experimental hypercholesterolemia in pigs and non-human primates stimulates the accumulation of inflammatory cells in the arterial adventitia. The extent of adventitial inflammation associated with human atherosclerotic plaques is correlated with the severity of intimal disease. Adventitial reactions also occur after balloon angioplasty. Our studies indicate that the major site of cell proliferation after angioplasty of porcine coronary arteries is the adventitia and not the medial wall. These cells have been identified as myofibroblasts on the basis of differential staining with smooth muscle specific antibodies and a role for these cells in arterial remodeling associated with angioplasty and late lumen loss is postulated. Evidence from pulse studies with bromodeoxyuridine suggests that adventitial myofibroblasts have the capacity to migrate into the forming intimal lesion after angioplasty and may be a major component of the neointima. Additional work will have to be directed at a more detailed examination of the response of adventitial cells to balloon injury and in the setting of atherosclerosis and arteritis to determine what role these cells might play vascular lesion development.

Angioplasty, Balloon, Coronary↗
PubMed2002

Targeting the adventitia with intracoronary beta-radiation: comparison of two dose prescriptions and the role of centering coronary arteries.

PURPOSE: To compare by intravascular ultrasound (IVUS) the efficacy of delivering the prescribed dose to the adventitia between two commonly used dose prescriptions for intracoronary radiotherapy. METHODS AND MATERIALS: In 59 human postangioplasty coronary vessels, one IVUS cross-section (1 mm thick) with the highest plaque burden was used for creating dose-volume histograms with different hypothetical positions of the source. RESULTS: On average, prescription to 1 mm beyond lumen surface resulted in delivery of the prescribed dose (20 Gy +/- 20%) to a higher fraction of adventitial volume than with the prescription to 2 mm from the source, with source placed in vessel center, lumen center, or in the IVUS catheter position. Source placement in the lumen center resulted in a low dose heterogeneity to the adventitia and the least dose heterogeneity to the intima. CONCLUSIONS: Prescription to 1 mm beyond lumen surface appeared more effective in delivering the prescribed dose to the adventitia than the American Association of Physicists in Medicine (AAPM) recommended prescription to 2 mm from the source center. Moreover, centering the source in the lumen provides the better balance of effective adventitial targeting and intimal dose homogeneity. Modification of the current AAPM recommendation for dose prescription for intracoronary radiotherapy should be considered.

Analysis of Variance↗
PubMed1997

Localization of a constitutively active, phagocyte-like NADPH oxidase in rabbit aortic adventitia: enhancement by angiotensin II.

Superoxide anion (O2-) plays a key role in the endogenous suppression of endothelium-derived nitric oxide (NO) bioactivity and has been implicated in the development of hypertension. In previous studies, we found that O2- is produced predominantly in the adventitia of isolated rabbit aorta and acts as a barrier to NO. In the present studies, we characterize the enzyme responsible for O2- production in the adventitia and show that this enzyme is a constitutively active NADPH oxidase with similar composition as the phagocyte NADPH oxidase. Constitutive O2--generating activity was localized to aortic adventitial fibroblasts and was enhanced by the potent vasoconstrictor angiotensin II. Immunohistochemistry of aortic sections demonstrated the presence of p22(phox), gp91(phox), p47(phox), and p67(phox) localized exclusively in rabbit aortic adventitia, coincident with the site of staining for O2- production. Furthermore, immunodepletion of p67(phox) from adventitial fibroblast particulates resulted in the loss of NADPH oxidase activity, which could be restored by the addition of recombinant p67(phox). Further study into the regulation of this adventitial source of O2- is important in elucidating the mechanisms regulating the bioactivity of NO and may contribute to our understanding of the pathogenesis of hypertension.

Angiotensin II↗
PubMed2006

Statistical strategy for anisotropic adventitia modelling in IVUS.

Vessel plaque assessment by analysis of intravascular ultrasound sequences is a useful tool for cardiac disease diagnosis and intervention. Manual detection of luminal (inner) and media-adventitia (external) vessel borders is the main activity of physicians in the process of lumen narrowing (plaque) quantification. Difficult definition of vessel border descriptors, as well as, shades, artifacts, and blurred signal response due to ultrasound physical properties trouble automated adventitia segmentation. In order to efficiently approach such a complex problem, we propose blending advanced anisotropic filtering operators and statistical classification techniques into a vessel border modelling strategy. Our systematic statistical analysis shows that the reported adventitia detection achieves an accuracy in the range of interobserver variability regardless of plaque nature, vessel geometry, and incomplete vessel borders.

Algorithms↗
PubMed2002

Mechanics of the human femoral adventitia including the high-pressure response.

Adventitial mechanics were studied on the basis of adventitial tube tests and associated stress analyses utilizing a thin-walled model. Inflation tests of 11 nonstenotic human femoral arteries (79.3 +/- 8.2 yr, means +/- SD) were performed during autopsy. Adventitial tubes were separated anatomically and underwent cyclic, quasistatic extension-inflation tests using physiological pressures and high pressures up to 100 kPa. Associated circumferential and axial stretches were typically <20%, indicating "adventitiosclerosis." Adventitias behaved nearly elastically for both loading domains, demonstrating high tensile strengths (>1 MPa). The anisotropic and strongly nonlinear mechanical responses were represented appropriately by two-dimensional Fung-type stored-energy functions. At physiological pressure (13.3 kPa), adventitias carry ~25% of the pressure load in situ, whereas their circumferential and axial stresses were similar to the total wall stresses (~50 kPa in both directions), supporting a "uniform stress hypothesis." At higher pressures, they became the mechanically predominant layer, carrying >50% of the pressure load. These significant load-carrying capabilities depended strongly on circumferential and axial in-vessel prestretches (mean values: 0.95 and 1.08). On the basis of these results, the mechanical role of the adventitia at physiological and hypertensive states and during balloon angioplasty was characterized.

Aged↗
PubMed2002

Selective expansion of fibroblast subpopulations from pulmonary artery adventitia in response to hypoxia.

Proliferation of fibroblasts contributes to the adventitial thickening observed during the development of hypoxia-induced pulmonary hypertension. However, whether all or only specific subpopulations of fibroblasts proliferate during this process is unknown. Because lung, skin, and gingiva contain multiple fibroblast subpopulations, we hypothesized that the pulmonary artery (PA) adventitia of neonatal calves is composed of multiple fibroblast subpopulations and that only selective subpopulations expand under chronic hypoxic conditions. Fibroblast subpopulations were isolated from PA adventitia of control calves using limited dilution cloning techniques. These subpopulations exhibited marked differences in morphology, actin expression, and serum-stimulated growth. Only select fibroblast subpopulations demonstrated the ability to proliferate in response to hypoxia. Fibroblast subpopulations were similarly isolated from calves exposed to hypoxia (14 days). With regard to morphology, actin expression, and serum-stimulated growth of subpopulations, there were no obvious differences in fibroblast subpopulations between the hypoxic and the control calves. However, the number of fibroblast subpopulations with about a twofold increase in hypoxia-induced DNA synthesis was significantly greater in the hypoxic calves (26%) compared with control calves (10%). We conclude that the bovine PA adventitia comprises numerous phenotypically and biochemically distinct fibroblast subpopulations and that select subpopulations expand in response to chronic hypoxia.

Animals↗
PubMed2001

Trophic effect of norepinephrine on arterial intima-media and adventitia is augmented by injury and mediated by different alpha1-adrenoceptor subtypes.

In vivo studies have suggested that norepinephrine (NE) directly contributes to normal vascular wall growth and worsening of hypertrophy, atherosclerosis, and restenosis. However, it is unknown whether these effects are secondary to hemodynamic changes caused by systemic NE or alpha-adrenoceptor (AR) antagonists. Herein, we determined if NE directly stimulates growth of medial smooth muscle cells (SMCs) and adventitial fibroblasts (AFBs) that we have shown express alpha1-ARs in similar abundance. The rat aorta was isolated before injury, 4 days after, or 12 days after balloon injury, and maintained under circumferential tension in organ culture for 48 hours with 1 micromol/L NE. Intima-media and adventitia were separated and DNA content, protein synthesis, and protein content measured. In uninjured aorta, NE increased DNA and protein content similarly in adventitia, and increased only protein content in intima-media, suggesting AFB proliferation and SMC hypertrophy. In vessels isolated 4 or 12 days after injury, NE increased all 3 endpoints in both layers by up to 20-fold greater than in uninjured vessels. These effects were dose-dependent and were unaffected by alpha2- or beta-AR blockade (except increased DNA content in adventitia that was also inhibited by alpha2-AR blockade). Intima-media growth was blocked by KMD3213 (alpha1A-AR antagonist) and adventitial growth by AH11110A (alpha1B-AR antagonist), whereas BMY7378 (alpha1D-AR antagonist) had no effect. NE decreased SMC marker proteins (eg, alpha-smooth muscle actin and desmin) and augmented the changes induced by injury. These data suggest that prolonged stimulation of alpha1A- and alpha1B-ARs induces growth of SMCs and AFBs, respectively, that is significantly augmented by injury.

Angiotensin II↗
PubMed2006

Paclitaxel delivered to adventitia attenuates neointima formation without compromising re-endothelialization after angioplasty in a porcine restenosis model.

PURPOSE: To investigate the effect of paclitaxel delivered into the adventitia of pig femoral arteries on neointima formation and hyperplasia as well as re-endothelialization. METHODS: Paclitaxel or vehicle was delivered into the adventitia of pig femoral arteries using a needle injection catheter following balloon overstretch. Arteries were then serially examined by angiography, Evan's blue staining, morphometry, and immunohistochemistry for up to 12 weeks. RESULTS: Local adventitial delivery of paclitaxel significantly attenuated neointima formation. The area of neointima (0.41+/-0.17 versus 2.75+/-0.81 mm(2), p<0.01), the ratio of intima to media (0.12+/-0.05 versus 0.86+/-0.35, p<0.05), and the degree of stenosis (12.80%+/-3.13% versus 47.06%+/-7.25%, p<0.01) were significantly lower in the paclitaxel-treated group compared to controls. Furthermore, cell proliferation was significantly diminished following adventitial delivery of paclitaxel from day 3 to 21 compared to controls. Complete re-endothelialization was observed 3 weeks after intervention in both groups of arteries treated with paclitaxel or vehicle alone. CONCLUSION: Paclitaxel delivered into the adventitia of pig femoral arteries effectively attenuates neointima formation after angioplasty without compromising re-endothelialization. Adventitial drug delivery may therefore be an alternative to drug-eluting stents for the prevention of restenosis.

Analysis of Variance↗
PubMed1997

[Histological study of the tracheal adventitia, perichondrium and annular ligament].

The trachea begins at the lower border of the cricoid cartilage and passes down to bifurcate into the left and right mainstem bronchi. The presence of tracheal invasion is crucial factor influencing the prognosis for patients with cancers of the thyroid gland, hypopharynx, esophagus, etc. In order to understand the manner of invasion of the above tumors, precise knowledge of the normal tracheal structure is indispensable. This study was undertaken to clarify the normal microscopic structure of the trachea. Five normal tracheal specimens obtained at surgery were examined histologically and immunohistochemically. The loose connective tissue around the trachea, known as adventitia, was divided into a loose outer and a dense inner layer by hematoxylin and eosin (HE) staining. This two-layer pattern was clearly seen near the annular ligament but was obscured away from it. The connective tissue of the inner layer ran obliquely to joint the connective tissue of the annular ligament and ended in the submucosal layer. This arrangement of connective fibers seems to play a role in allowing the trachea to stretch and bend. Tracheal cartilage is covered with a dense fibrous membrane known as the perichoundrium. Between the superficial fibrous membrane and mature cartilage cells lies zone of immature cartilage made up of oval or spindle cells, and the inclusion of this zone in the perichondrium has long been a subject of controversy. In our study, the zone was homogeneously stained red by the elastica van Gieson's stain and was clearly distinguished from other structures. Immunohistochemical staining revealed a wide distribution of type I and type III collagen on the fibrous membrane and the zone of immature cartilage cells, while mature cartilage cells did not show such collagen. Based on these findings, we conclude that the zone of immature cartilage cells belongs to the periochondrium, which thus contains two layers, an outer fibrous layer and an inner transitional layer of immature cartilage cells. Our conclusions are as follows: 1. Tracheal adventitia is divided into two layers, an outer loose and an inner dense fibrous layer. 2. Tracheal perichondrium also consists of two layers, an outer fibrous layer and an inner transitional layer. 3. The fibrous bundle originating from the adventitia joins the connective tissue of the annular ligament, probably in order to allow the trachea to stretch and bend.

Collagen↗
PubMed1976

[Relationship between the thickness of the aortic adventitia and the fat content of blood and the aortic wall].

10 rabbits underwent a cholesterol feeding. 10 rabbits were used as control animals. After 12 weeks in the tissue extract of the intima-media-complex of the aorta as well as in the serum the total lipids and the total cholesterol were determined. On histological preparations the thickness of the adventitia of the aorta was measured. In comparison to the control group the animals fed with cholesterol showed a significant increase of the lipid values in the serum and the aorta as well as of the thickness of the adventitia. However, no connections could be proved between the parameters of the serum lipids and the morphological changes of the adventitia.

Animals↗
PubMed1997

Expression of two novel recombinant proteins from aortic adventitia (kappafibs) sharing amino acid sequences with cytomegalovirus.

We have recently purified and partially sequenced a microfibrillar protein from human aortic adventitia (aneurysm-associated antigenic protein, 40 kDa [AAAP-40]) that is immunoreactive with immunoglobulin (IgG) from the wall of abdominal aortic aneurysms (AAAs). It shares motifs with Ig kappa (which may act as a binding site for interaction with integrins), cytomegalovirus (which may be a molecular mimic in the pathogenesis of AAA), and vitronectin and the fibrinogens. A cDNA library was constructed from the aortic adventitia of a AAA. The library was screened with either rabbit anti-vitronectin antibody or rabbit anti-fibrinogen antibody. Positive plaques were purified and expressed in a strain of Escherichia coli. The clone sequences were analyzed. The expressed proteins were separated by SDS/PAGE and the immunoblots were probed with either AAA IgG or anti-human Ig kappa antibody. Experimental cell lines, transfected with the clones (clones 1 and 5), synthesized recombinant proteins (rAAAP-CL1 and rAAAP-CL5), detectable in Western immunoblots with AAA IgG. A prediction of the tertiary structure resembles well-characterized cell adhesion molecules. These findings suggest that there is a novel family of matrix proteins that may use immunoglobulin motifs as binding sites for cellular integrins and that there are matrix proteins in addition to AAAP-40 that may serve as autoantigens in the pathogenesis of AAA disease.

Amino Acid Sequence↗
PubMed1995

Selective coagulation necrosis of canine adventitia and media induces extracellular matrix accumulation without neointima formation.

Endothelial cell injury, the disruption of the internal elastic membrane and medial damage represent important stimuli for the development of a neointima. It is unclear whether selective adventitial and medial injury also induce neointima formation. Incremental argon laser energies (11.4-180 J/cm2) were applied to the external surface of dog femoral arteries to evaluate the vascular repair of acute adventitial or medial necrosis without injury of the intima. The animals were sacrificed either one hour after the initial procedure or after an 8 week follow up period for histologic examination. Acute, and mild to moderate necrosis of the arterial wall was found above 50 J/cm2. Ablation of the internal elastic membrane or mural thrombi was not detected. Eight weeks after photocoagulation with laser energies above 50 J/cm2, a significant increase in mean wall thickness of the media was observed. The medial thickening was characterised by an accumulation of extracellular matrix and a loss of smooth muscle cells. Necrosis of adventitia and media resulted in arterial wall thickening without neointima formation. It is concluded that, in dogs, an acute, selective injury of adventitia and media stimulates the production of extracellular matrix and not the proliferation of cells. Smooth muscle cell migration and subsequently neointima formation are induced by viable smooth muscle cells when blood-borne stimuli are available.

Analysis of Variance↗
PubMed1994

The adventitia and atherogenesis: removal initiates intimal proliferation in the rabbit which regresses on generation of a 'neoadventitia'.

Removal of the carotid artery adventitia from rabbits induced the formation of an intimal hyperplastic lesion. In rabbits fed a normal diet, the lesion (measured as the intimal:medial ratio) was maximal by day 14 (0.456 +/- 0.079, n = 5, P < 0.01) and thereafter, regressed towards control dimensions (0.037 +/- 0.003, n = 14) by day 28 (0.080 +/- 0.025, n = 7, P = 0.14). In rabbits fed a high cholesterol diet, the lesion was again maximal by day 14 (0.376 +/- 0.056, n = 8, P < 0.01). Although some regression was seen, the lesion persisted to day 42 (0.272 +/- 0.052, n = 8, P < 0.01). Electron microscopy and immunocytochemistry showed two types of lesion, (a) smooth muscle cell predominant on normal diet and, (b) macrophage predominant on high cholesterol diet. Smooth muscle cell predominant lesions underwent almost complete regression, whereas macrophage predominant lesions persisted. We propose that lesion formation may be initiated following the development of arterial wall hypoxia, secondary to excision of the adventitial vasa vasorum. Furthermore, we have devised a novel method to restore a highly vascular 'neoadventitia' to an artery whose adventitia has previously been removed, using loosely placed PVC tubing. We suggest this 'neoadventitia' was able to inhibit the formation of an intimal hyperplastic lesion and to promote regression of an already established lesion by restoring arterial wall oxygenation.

Animals↗
PubMed1997

The discovery and a study of the adventitia rectalis, a fibrous layer of the rectal wall.

In sacral anoplasty, it is frequently found that an outer layer of the rectal wall, which resembles the structure of the taenia bands of the colon, limits the elasticity of the rectum making it different from the small intestine, hence preventing the rectal stump from being advanced to reach the perineum. Results of autopsy studies on 40 human babies and 40 dogs showed that a special collagenous fibrous layer called adventitia rectalis was found to limit the free expansion of the rectal wall. This was responsible for keeping the rectum a straight tubular shape with a fixed volume. This tissue plays an important role in bowel movement by defining a threshold of intrarectal pressure in the bowel reflex of defecation and by transmitting the expulsive force from the abdomen above down to the anal opening. This discovery may explain why (1) in Hirschsprung's disease, the preservation of the rectal wall in Soave's or Rehbein's procedure or partial preservation in Duhamel's operation will preserve better bowel function; (2) in atresia ani, rectal tapering results in better bowel control than rectal pouch amputation; and (3) in sacral anoplasty, multiple releasing incisions of adventitia rectalis at different levels will lengthen the rectal stump to about double its original length to reach the perineal incision, and the divided fibers will soon regenerate.

Anal Canal↗
PubMed1999

Adventitia as a source of inducible nitric oxide synthase in the rat aorta.

In the current study we used in vitro and in vivo models to determine the sites of nitric oxide production in rat aortic tissue following cytokine stimulation. In vitro studies in which intact rat aortic rings were incubated with endotoxin (1 microg/mL) or interferon-gamma (600 U/mL) indicated that the expression of inducible nitric oxide synthase (iNOS) activity was increased as measured by Northern blot analysis or determination of nitrite production. In situ hybridization showed iNOS mRNA in the endothelium and adventitia of the incubated aortic rings but not in the media. Immunohistochemical staining showed a similar localization for iNOS protein in the incubated rings. Additional studies were performed in which bacterial endotoxin (4 mg/kg) was administered to rats, and iNOS expression was assayed using in situ hybridization and immunohistochemistry. Clear increases in iNOS mRNA and protein were found in aortic tissue. Endothelial and adventitial cells were the major source of iNOS, with relatively low amounts of iNOS mRNA present in medial smooth muscle, consistent with in vitro findings. These studies indicate that the aortic adventitia is a potential source of NO, and suggest that the adventitial fibroblast may have an important paracrine role in regulating arterial structure and function.

Animals↗
PubMed1997

Acute and chronic in vivo inhibition of angiotensin-converting enzyme by perindopril in the endothelium and adventitia of large arteries and organs of the rabbit.

Angiotensin-converting enzyme (ACE) inhibitors are widely used in treating hypertension and chronic heart failure, but their precise sites and mechanisms of the actions are not completely understood. In this study, we evaluated the acute and chronic in vivo inhibition of ACE by perindopril in both the endothelium and adventitia of large blood vessels including the aorta, carotid, and femoral arteries, heart, lung, and kidney by using in vitro autoradiography with [(125)I]351A as a ligand. After short-term (0.1, 0.3, and 1 mg/kg) or long-term oral administration (0.3 mg/kg), perindopril significantly inhibited plasma ACE (p < 0.001), the plasma angiotensin II (Ang II)/Ang I ratio (p < 0.01), and decreased mean arterial pressure (p < 0.001) in a dose-related manner. In the aorta, carotid, and femoral arteries, free ACE was inhibited to a similar extent in both the endothelium and adventitia by perindopril, in a dose-dependent manner, whereas total ACE in both layers of these vessels was unaltered. Similar short- and long-term ACE inhibition by perindopril was observed in the lung and heart, with somewhat greater inhibition of kidney and plasma ACE. Vascular and tissue ACE inhibition correlated highly with both plasma ACE and the plasma Ang II/Ang I ratio (r = 0.63-0.89; p < 0.001). Whereas the effects of perindopril on blood pressure, plasma Ang II/Ang I ratio, plasma and vascular ACE were all highly dose dependent, there were no significant differences on the degree of ACE inhibition observed between the three large blood vessels or between their adventitial and endothelial layers. These results demonstrate that perindopril readily penetrates the vascular wall after short- or long-term oral administration, and in a dose-dependent manner, potently inhibits both endothelial and advential vascular ACE to a comparable degree. Therefore ACE inhibitors may be beneficial in inhibiting both circulating Ang II and its local formation in the vascular wall.

Angiotensin I↗